Evaluation of muscle-specific and metabolism regulating microRNAs in a chronic swimming rat model.

IF 1.8 3区 生物学 Q4 CELL BIOLOGY
Zsuzsanna Gaál, János Fodor, Attila Oláh, Tamás Radovits, Béla Merkely, János Magyar, László Csernoch
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引用次数: 1

Abstract

Making benefit from the epigenetic effects of environmental factors such as physical activity may result in a considerable improvement in the prevention of chronic civilization diseases. In our chronic swimming rat model, the expression levels of such microRNAs were characterized, that are involved in skeletal muscle differentiation, hypertrophy and fine-tuning of metabolism, which processes are influenced by chronic endurance training, contributing to the metabolic adaptation of skeletal muscle during physical activity. After chronic swimming, the level of miR-128a increased significantly in EDL muscles, which may influence metabolic adaptation and stress response as well. In SOL, the expression level of miR-15b and miR-451 decreased significantly after chronic swimming, which changes are opposite to their previously described increment in insulin resistant skeletal muscle. MiR-451 also targets PGC-1α mRNA, whiches expression level significantly increased in SOL muscles, resulting in enhanced biogenesis and oxidative capacity of mitochondria. In summary, the microRNA expression changes that were observed during our experiments suggest that chronic swim training contributes to a beneficial metabolic profile of skeletal muscle.

Abstract Image

Abstract Image

Abstract Image

慢性游泳大鼠模型中肌肉特异性和代谢调节microrna的评价。
利用身体活动等环境因素的表观遗传效应,可以在预防慢性文明疾病方面取得相当大的进步。在我们的慢性游泳大鼠模型中,表征了这些microrna的表达水平,这些microrna参与骨骼肌分化、肥大和代谢微调,这些过程受到慢性耐力训练的影响,有助于骨骼肌在体育活动期间的代谢适应。在长期游泳后,EDL肌肉中miR-128a水平显著升高,这也可能影响代谢适应和应激反应。在SOL中,长期游泳后miR-15b和miR-451的表达水平显著下降,这一变化与之前描述的胰岛素抵抗骨骼肌中miR-15b和miR-451的增加相反。MiR-451还靶向PGC-1α mRNA, PGC-1α mRNA在SOL肌肉中的表达水平显著升高,导致线粒体的生物发生和氧化能力增强。总之,在我们的实验中观察到的microRNA表达变化表明,长期游泳训练有助于骨骼肌的有益代谢谱。
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来源期刊
CiteScore
6.20
自引率
0.00%
发文量
21
审稿时长
>12 weeks
期刊介绍: The Journal of Muscle Research and Cell Motility has as its main aim the publication of original research which bears on either the excitation and contraction of muscle, the analysis of any one of the processes involved therein, the processes underlying contractility and motility of animal and plant cells, the toxicology and pharmacology related to contractility, or the formation, dynamics and turnover of contractile structures in muscle and non-muscle cells. Studies describing the impact of pathogenic mutations in genes encoding components of contractile structures in humans or animals are welcome, provided they offer mechanistic insight into the disease process or the underlying gene function. The policy of the Journal is to encourage any form of novel practical study whatever its specialist interest, as long as it falls within this broad field. Theoretical essays are welcome provided that they are concise and suggest practical ways in which they may be tested. Manuscripts reporting new mutations in known disease genes without validation and mechanistic insight will not be considered. It is the policy of the journal that cells lines, hybridomas and DNA clones should be made available by the developers to any qualified investigator. Submission of a manuscript for publication constitutes an agreement of the authors to abide by this principle.
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